PMID- 7539030
OWN - NLM
STAT- MEDLINE
DCOM- 19950628
LR  - 20220309
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 57
IP  - 5
DP  - 1995 May
TI  - A role for C-C chemokines in fibrotic lung disease.
PG  - 782-7
AB  - Pulmonary fibrosis is the end point of a chronic inflammatory process 
      characterized by leukocyte recruitment and activation, fibroblast proliferation, 
      and increased extracellular matrix production. Previous studies of models of 
      pulmonary fibrosis have investigated the role of cytokines in the evolution of 
      the fibrotic response. The involvement of tumor necrosis factor and interleukin-1 
      in bleomycin-induced lung injury, a model of idiopathic pulmonary fibrosis, has 
      been well established, suggesting that cytokines mediate the initiation and 
      maintenance of chronic inflammatory lesions. However, the aforementioned 
      cytokines alone cannot account for the recruitment and activation of specific 
      leukocyte populations found in the bleomycin model. Recently, a family of novel 
      proinflammatory cytokines (chemokines) was cloned and characterized, yielding 
      many putative mediators of leukocyte functions. Macrophage inflammatory protein-1 
      alpha (MIP-1 alpha) and monocyte chemoattractant protein-1 (MCP-1) belong to the 
      C-C chemotactic cytokine family, a group of low-molecular-weight peptides. These 
      molecules modulate chemotaxis, proliferation, and cytokine expression in 
      leukocyte subsets. Our group has investigated the roles of MCP-1 and MIP-1 alpha 
      in the bleomycin model. Both MCP-1 and MIP-1 alpha are expressed in a 
      time-dependent manner after bleomycin challenge, and passive immunization of 
      these animals with either anti-MIP-1 alpha or anti-MCP-1 antibodies attenuated 
      leukocyte accumulation. In addition, we have identified specific cell types 
      expressing MCP-1 or MIP-1 alpha by in situ hybridization and immunohistochemical 
      localization, respectively. Furthermore, our results indicate that MIP-1 alpha 
      expression is mediated by alveolar macrophage-derived tumor necrosis factor, 
      identifying an important cytokine pathway in the initiation of pulmonary 
      fibrosis. Finally, anti-MIP-1 alpha therapy attenuated fibrosis, providing direct 
      evidence for its involvement in fibrotic pathology. Our work has clearly 
      established that the C-C chemokines MCP-1 and MIP-1 alpha are expressed and 
      contribute to the initiation and maintenance of the bleomycin-induced pulmonary 
      lesion.
FAU - Smith, R E
AU  - Smith RE
AD  - Department of Pathology, University of Michigan Medical School, Ann Arbor 
      48109-0602, USA.
FAU - Strieter, R M
AU  - Strieter RM
FAU - Zhang, K
AU  - Zhang K
FAU - Phan, S H
AU  - Phan SH
FAU - Standiford, T J
AU  - Standiford TJ
FAU - Lukacs, N W
AU  - Lukacs NW
FAU - Kunkel, S L
AU  - Kunkel SL
LA  - eng
GR  - HL02401/HL/NHLBI NIH HHS/United States
GR  - HL28737/HL/NHLBI NIH HHS/United States
GR  - HL31693/HL/NHLBI NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Cytokines)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (Monocyte Chemoattractant Proteins)
RN  - 0 (Monokines)
RN  - 11056-06-7 (Bleomycin)
SB  - IM
MH  - Bleomycin/*adverse effects
MH  - Chemokine CCL4
MH  - Chemotactic Factors/physiology
MH  - Cytokines/*physiology
MH  - Fibroblasts/physiology
MH  - Humans
MH  - Lymphocytes/*physiology
MH  - Macrophage Inflammatory Proteins
MH  - Macrophages/*physiology
MH  - Monocyte Chemoattractant Proteins
MH  - Monokines/physiology
MH  - Neutrophils/physiology
MH  - Pulmonary Fibrosis/*physiopathology
RF  - 57
EDAT- 1995/05/01 00:00
MHDA- 1995/05/01 00:01
CRDT- 1995/05/01 00:00
PHST- 1995/05/01 00:00 [pubmed]
PHST- 1995/05/01 00:01 [medline]
PHST- 1995/05/01 00:00 [entrez]
AID - 10.1002/jlb.57.5.782 [doi]
PST - ppublish
SO  - J Leukoc Biol. 1995 May;57(5):782-7. doi: 10.1002/jlb.57.5.782.